5-5--6-6--tetrachloro-1-1--3-3--tetraethylbenzimidazolocarbocyanine has been researched along with Osteosarcoma* in 2 studies
2 other study(ies) available for 5-5--6-6--tetrachloro-1-1--3-3--tetraethylbenzimidazolocarbocyanine and Osteosarcoma
| Article | Year |
|---|---|
Influence of a mitochondrial genetic defect on capacitative calcium entry and mitochondrial organization in the osteosarcoma cells.
Effects of T8993G mutation in mitochondrial DNA (mtDNA), associated with neurogenical muscle weakness, ataxia and retinitis pigmentosa (NARP), on the cytoskeleton, mitochondrial network and calcium homeostasis in human osteosarcoma cells were investigated. In 98% NARP and rho(0) (lacking mtDNA) cells, the organization of the mitochondrial network and actin cytoskeleton was disturbed. Capacitative calcium entry (CCE) was practically independent of mitochondrial energy status in osteosarcoma cell lines. The significantly slower Ca(2+) influx rates observed in 98% NARP and rho(0), in comparison to parental cells, indicates that proper actin cytoskeletal organization is important for CCE in these cells. Topics: Actins; Ataxia; Benzimidazoles; Calcium; Carbocyanines; Carbonyl Cyanide m-Chlorophenyl Hydrazone; Cell Line, Tumor; Cytoskeleton; DNA, Mitochondrial; Fluorescent Dyes; Fura-2; Humans; Image Processing, Computer-Assisted; Immunohistochemistry; Ionophores; Membrane Potentials; Microscopy, Fluorescence; Mitochondrial Myopathies; Muscle Weakness; Mutation; Osteosarcoma; Phalloidine; Retinitis Pigmentosa; Rhodamines; Thapsigargin | 2004 |
Mitochondrial permeability transition and swelling can occur reversibly without inducing cell death in intact human cells.
Severe disruption of mitochondrial function is generally considered to provide a powerful trigger for apoptosis in mammalian cells. We report here that intact cells may undergo the mitochondrial permeability transition and mitochondria swell in a fully reversible manner, without inducing cell death. Cultured human osteosarcoma cells (143B TK-) stained with JC-1, MitoTracker dyes, or calcein plus Co2+ were imaged by confocal microscopy to visualize changes of mitochondrial membrane potential (DeltaPsim), morphology, and permeability transition, respectively, during treatment with a protonophore, carbonyl cyanide m-chlorophenylhydrazone (CCCP). Cells rapidly exhibited mitochondrial permeability transition and swelling after addition of CCCP, but the swelling subsided within hours, leaving mitochondria that appeared in punctate form, not filamentous as before CCCP treatment. Cyclosporin A impeded the permeability transition and swelling, although complete inhibition was not observed. Cells survived the dissipation of DeltaPsim by CCCP for up to 6 h without developing any obvious cell damage or signs of apoptosis. With the restoration of DeltaPsim after removal of CCCP (following 6 h of CCCP treatment), permeability transition pores were closed. These results suggest that none of the following events represent a point of no return in the process of apoptotic cell death: loss of DeltaPsim, mitochondrial permeability transition, or mitochondrial swelling. Topics: Aldehydes; Apoptosis; Benzimidazoles; Carbocyanines; Carbonyl Cyanide m-Chlorophenyl Hydrazone; Cell Survival; Cyclosporine; Fluoresceins; Fluorescent Dyes; Humans; Intracellular Membranes; Ionophores; Membrane Potentials; Microscopy, Confocal; Mitochondria; Mitochondrial Swelling; Organic Chemicals; Osteosarcoma; Permeability; Staining and Labeling; Tumor Cells, Cultured | 1999 |